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Query: UMLS:C0155339 (Brown)
 12,436 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Deoxycorticosterone acetate (DOCA)-salt hypertension was induced in Brown Norway (BN) kininogen-deficient rats (BN-Ka) and normal rats from the same strain (BN-Ki) after nephrectomy. Systolic blood pressure, which was determined by the tail-cuff method, of BN-Ki increased gradually during this treatment. In contrast, the blood pressure of mutant BN-Ka increased rapidly 2 weeks after the onset of the treatment. Urinary excretion of active kallikrein and prokallikrein increased at the same degree in rats of both strains during this treatment. Significant increase in urinary sodium excretion was observed with a tendency to increase in urine volume during the treatment in normal BN-Ki rats, whereas both parameters were essentially not increased in mutant BN-Ka rats, which could not generate urinary kinin. Aprotinin infusion by osmotic minipump to normal BN-Ki rats during the DOCA-salt treatment resulted in significant further increase in the systolic blood pressure.
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PMID:Essential role of kallikrein-kinin system in suppression of blood pressure rise during the developmental stage of hypertension induced by deoxycorticosterone acetate-salt in rats. 128 79

It has recently been proposed that sequence variation in the gene coding for tissue kallikrein might be involved in the pathogenesis of hypertension. However, molecular evidence of an association between a sequence alteration in the kallikrein gene family and the transmission of increased blood pressure has never been reported. In 32 recombinant inbred (RI) strains derived from the spontaneously hypertensive rat (SHR) and the normotensive Brown Norway rat (BN), we investigated whether a restriction fragment length polymorphism (RFLP) marking the kallikrein gene family cosegregated with blood pressure. In the RI strains that inherited the kallikrein RFLP from the SHR progenitor strain, the median systolic, diastolic, and mean arterial pressures were significantly greater than in the RI strains that inherited the kallikrein RFLP from the BN progenitor strain. These findings suggest that in the rat, sequence variation in the kallikrein gene family, or in closely linked genes, may have the capacity to affect blood pressure.
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PMID:Cosegregation of blood pressure with a kallikrein gene family polymorphism. 167 81

We studied the influence of aprotinin and soya bean trypsin inhibitor (SBTI) on the inflammatory reaction induced by the implantation of dry sponges in normal Wistar rats and in kininogen-deficient Brown Norway rats, during the first day after the implantation. In normal rats, aprotinin reduced the volume and total protein content of the exudates at 3 h but not thereafter. Aprotinin also markedly reduced the immunoreactive kinins and kallikrein in the exudates. Aprotinin did not modify the volume of the exudates of the Brown Norway rats. SBTI reduced the inflammatory reaction in both rat strains but did not significantly modify the formation of immunoreactive kinins. The inflammatory reaction developed more slowly in Brown Norway rats. The kinin system is thus involved during the first hours of the development of this acute inflammatory reaction. The anti-inflammatory effect of SBTI does not depend on the inhibition of kinin formation.
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PMID:Proteinase inhibitors, kinins and the inflammatory reaction induced by sponge implantation in rats. 169 Nov 1

Brown Norway kininogen-deficient rats had very low levels of plasma kininogens and lower levels of plasma prekallikrein, compared with those of normal rats of the same strain. Systolic blood pressure, determined by the tail-cuff method, of 5-week-old kininogen-deficient rats (106 +/- 0.4 mm Hg, n = 7) and the rate of systolic blood pressure increase with age were not different from those in normal rats. Weekly injections of deoxycorticosterone acetate (5 mg/kg s.c.) with 1% sodium chloride solution in drinking water after uninephrectomy at 7 weeks of age caused a gradual increase in the blood pressure of normal rats, reaching a plateau at 18 weeks of age, whereas that of deficient rats rose rapidly to 158 +/- 6 mm Hg 2 weeks after the start of treatment and continued to increase slightly, becoming significantly higher than normal rats at 8, 9, 10, 11, and 12 weeks of age (p less than 0.05 or 0.01). The levels of urinary prokallikrein and active kallikrein were slightly higher in deficient rats before deoxycorticosterone acetate-salt treatment but were not significantly increased after this treatment, whereas these levels in normal rats were increased 3.6- and 4.7-fold by this treatment. Urinary free kinin, collected from the ureter in untreated deficient rats, was below the detection limit. The plasma level of low molecular weight kininogen, the substrate of glandular kallikrein, was decreased in normal rats during the treatment. Continuous subcutaneous injection of aprotinin by an osmotic pump to normal rats induced significant increase in blood pressure. These results indicate that glandular kallikrein may play a suppressive role in deoxycorticosterone acetate-salt hypertension.
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PMID:Suppression of rat deoxycorticosterone-salt hypertension by kallikrein-kinin system. 171 Jun 5

Vasoactive hormones acting as endocrine, neuroendocrine, or local hormonal systems (intracrine, autocrine, and paracrine) are an important component of the many factors that regulate blood pressure. Hypertension may be the result of an alteration in the balance between vasodepressor and vasopressor hormonal systems. Changes in this balance could be due to genetic factors such as mutations in one of the genes of the vasoactive system or environmental factors that alter the synthesis and release of one or more vasoactive hormones. Endocrine and neuroendocrine vasopressor hormonal systems, such as the renin-angiotensin system and catecholamines, play a well-established and important role in the regulation of blood pressure and the pathogenesis of some secondary forms of hypertension. The blockade of such systems has already resulted in effective antihypertensive treatment. The role of local hormonal systems is less well established; however, recent evidence suggests they also play an important role in the regulation of blood pressure and the pathogenesis of hypertension. Some vasopressor hormonal systems, such as the renin-angiotensin system, can act as both endocrine or local hormonal systems. Work using transgenic rats harboring the mouse Ren-2 gene has conclusively demonstrated that the renin-angiotensin system, acting as a local hormonal system, has the capability to cause severe hypertension. Whether this model of experimental hypertension mimics any type of human hypertension is not known. Vasodepressor hormones such as kinins, prostaglandins, and endothelium-derived relaxing factor (EDRF) act mainly as local hormonal systems, with the notable exception of atrial natriuretic factor, which may act as both an endocrine and a local hormone. The tissue kallikrein-kinin system, acting either directly or via paracrine eicosanoids or EDRF, participates in local regulation of the circulation, renal function, and the acute antihypertensive effect of angiotensin converting enzyme inhibitors. A restriction fragment length polymorphism (RFLP) that distinguishes the kallikrein gene family of a strain of spontaneously hypertensive rats (SHR) from normotensive Brown Norway rats has been identified. In a set of 32 recombinant inbred strains derived from these SHR and Brown Norway strains, the RFLP marking the kallikrein gene family of SHR cosegregated with an increase in blood pressure. Also, in a study of Utah families it was found that a dominant-allele kallikrein gene expressed as high urinary kallikrein excretion was associated with a decreased risk of essential hypertension. In conclusion, vasopressor and vasodepressor hormones, acting not only as endocrine but also as local hormones, play an important role in the regulation of blood pressure and the pathogenesis of hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Local hormonal factors (intracrine, autocrine, and paracrine) in hypertension. 188 59

Paw oedema in the rat by carrageenin and kaolin partially caused by Hageman factor activation was potentiated by the new angiotensin converting enzyme (ACE) inhibitor 2-[N-[(S)-1-ethoxycarbonyl-3-phenylpropyl-L-alanyl]-(lS,3S,5S)-2- azabicyclo[3.3.0]octane-3-carboxylic acid] (ramipril, Hoe 498) due to its inhibition of kininase II which results in increased bradykinin levels. A dose of 1 microgram ramipril injected into the hind paw of Sprague-Dawley rats concomitantly with, or 1 mg/kg given orally 30 min before administration of the irritants, led to significantly increased inflammatory reactions. The same effects were observed when ramipril was administered 3 h after carrageenin. In the kallikrein-kinin-deficient Brown-Norway rat strain Mai Pfd/f, ramipril did not significantly alter the paw oedema induced as described above. In addition, pretreatment of Sprague-Dawley rats with 10 mg/kg i.v. bromelains completely prevented the potentiation of inflammation by ramipril. Paw oedema provoked by the Hageman factor non-activators serotonin, dextran, ovalbumin and anti-rat IgG was not potentiated by ramipril. The chronic adjuvant arthritis in Lewis rats was not influenced by daily oral treatment with 0.1-3 mg/kg ramipril. Thus, in the rat only those inflammatory reactions involving kinins, presumably generated by Hageman factor activators, are potentiated by ramipril and presumably by other ACE-inhibitors.
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PMID:Influence of the new angiotensin converting enzyme inhibitor ramipril on several models of acute inflammation and the adjuvant arthritis in the rat. 302 36

Catechin dimers induce a large long-lasting oedema when injected in the paw of the rat. This oedema is not inhibited by methysergide, promethazine, indomethacin, phenidone, bromophenacyl bromide and colchicine. It is not modified in rats made leukopenic by methotrexate. It is slightly delayed in Brown Norway rats which were kallikrein-kininogen deficient. Similarly catechin dimers induce the formation of a large peritoneal exudate in the rat. The exudate contains insignificant levels of leucocytes and 5-hydroxytryptamine. It contains kinins but its PG content is very low. The exudate does not activate (14C)-arachidonic acid into PG. Catechin dimers induce kinin formation in rat plasma "in vitro". They inhibit the formation of PG and HETE-like compounds from (14C)-arachidonic acid by rat peritoneal cells "in vitro". Catechin dimers administered at sub-irritant doses reduced carrageenan-induced oedema. Catechin dimers at low doses have an anti-inflammatory effect which may depend on PG synthesis inhibition. At larger doses, they induce inflammatory responses which occur with almost complete lack of participation of PG.
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PMID:Pro-inflammatory flavonoids which are inhibitors of prostaglandin biosynthesis. 392 75

The plasma of a peculiar strain of Brown Norway rats (BN/May Pfd f) is devoid of high molecular weight kininogen and poor in kallikrein. This strain could be used to estimate the involvement of the kinin system in inflammatory processes. In these rats, the oedema induced by kaolin, carrageenans, uric acid and urate crystals exhibited a small development, while the oedemas induced by 48/80, dextran, zymosan, trypsin, nystatin, concanavalin A and heating were not reduced. The exudates withdrawn from Brown Norway rats contained no kinin and a low level of PGE2. The involvement of the kinin system in these inflammatory models is discussed.
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PMID:The role of the kinin system in various inflammatory models in the rat. 651 19

A gel filtration profile of the plasma of Brown Norway Katholiek (B/N-Ka) rat was compared with those of B/N-Kitasato (B/N-Ki) and Sprague-Dawley (SD) rats. In the chromatograms of B/N-Ki and SD rat plasmas, high-molecular weight (HMW) kininogen was eluted together with pre-kallikrein. In lower molecular weight fractions, there were two kininogens, one of which released kinin by urinary kallikrein, snake venom kininogenase (SVK) and trypsin, and the other released kinin only by trypsin. In the chromatogram of B/N-Ka rat plasma, there was no fraction which released kinin by plasma kallikrein, urinary kallikrein or SVK. However, the kinin-release only by trypsin was found in the lower molecular weight fraction, which corresponds to the third peak of kininogen in the chromatograms of B/N-Ki and SD rat plasmas. These results indicate that B/N-Ka rat plasma is deficient in HMW kininogen, and also deficient in the LMW kininogen susceptible to urinary kallikrein and SVK, but it contains the third kininogen responsive only to trypsin.
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PMID:Demonstration of the third kininogen in high and low molecular weight kininogens-deficient Brown Norway Katholiek rat. 657 Mar 69

1. The oedema induced in the paw of the Wistar rat by local injection of three different carrageenans allows us to determine the inflammatory activity of these sulphated polysaccharides. This activity is greatest for the lambda type, it is reduced for the iota compound and is smallest for the kappa carrageenan. 2. Reduction of plasmatic stores of kininogens by ellagic acid or inhibition of kinin formation by hexadimethrine reduce the inflammatory reaction induced by the three carrageenans. Inhibition of kininases by phenanthroline increases the oedema. Thus the kinin system is involved in the development of this type of oedema. 3. In Brown-Norway rats, which lack of plasmatic kallikrein and kininogens, the inflammatory activity of the three carrageenans is very small. By comparing the activity in Wistar rats and in Brown-Norway rats, it is concluded that the kinin system is the most important factor in the development of the inflammatory reaction induced by the three types of carrageenans.
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PMID:[Kinins and oedema induced by different carrageenans (author's transl)]. 709 85


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